J R Chaganti1, A Heinecke2, T M Gates3, K J Moffat4, B J Brew5,6. 1. From the Departments of Radiology (J.R.C., K.J.M.) joga.chaganti@svha.org.au. 2. Brain Innovation B.V. (A.H.), Maastricht, the Netherlands. 3. Department of Neurology, Clinical Research Program (T.M.J.). 4. From the Departments of Radiology (J.R.C., K.J.M.). 5. Neurology (B.J.B.), St Vincent's Hospital, Darlinghurst, Sydney, New South Wales, Australia. 6. Neurosciences Program, Peter Duncan Neurosciences Unit (B.J.B.), St Vincent's Centre for Applied Medical Research, University of New South Wales, Sydney, Australia.
Abstract
BACKGROUND AND PURPOSE: HIV-associated neurocognitive disorder still occurs despite virally suppressive combination antiretroviral therapy. In the pre-combination antiretroviral era and in patients without HIV suppression, HIV-associated neurocognitive disorder was caused by synaptodendritic injury resulting in impairment of neural networks, characterized by decreased attention, psychomotor slowing, and working memory deficits. Whether similar pathogenesis is true for HIV-associated neurocognitive disorder in the context of viral suppression is not clear. Resting-state fMRI has been shown to be efficient in detecting impaired neural networks in various neurologic illnesses. This pilot study aimed to assess resting-state functional connectivity of the brain in patients with active HIV-associated neurocognitive disorder in the context of HIV viral suppression in both blood and CSF. MATERIALS AND METHODS: Eighteen patients with active HIV-associated neurocognitive disorder (recent diagnosis with progressing symptoms) on combination antiretroviral therapy with viral suppression in both blood and CSF and 9 demographically matched control subjects underwent resting-state functional MR imaging. The connectivity in the 6 known neural networks was assessed. To localize significant ROIs within the HIV and control group, we performed a seed-based correlation for each known resting-state network. RESULTS: There were significant group differences between the control and HIV-associated neurocognitive disorder groups in the salience (0.26 versus 0.14, t = 2.6978, df = 25, P = .0123) and executive networks (0.52 versus 0.32, t = 2.2372, df = 25, P = .034). The covariate analysis with neuropsychological scores yielded statistically significant correlations in all 6 studied functional networks, with the most conspicuous correlation in salience networks. CONCLUSIONS: Active HIV-associated neurocognitive disorder in virally suppressed patients is associated with significantly decreased connectivity in the salience and executive networks, thereby making it potentially useful as a biomarker.
BACKGROUND AND PURPOSE:HIV-associated neurocognitive disorder still occurs despite virally suppressive combination antiretroviral therapy. In the pre-combination antiretroviral era and in patients without HIV suppression, HIV-associated neurocognitive disorder was caused by synaptodendritic injury resulting in impairment of neural networks, characterized by decreased attention, psychomotor slowing, and working memory deficits. Whether similar pathogenesis is true for HIV-associated neurocognitive disorder in the context of viral suppression is not clear. Resting-state fMRI has been shown to be efficient in detecting impaired neural networks in various neurologic illnesses. This pilot study aimed to assess resting-state functional connectivity of the brain in patients with active HIV-associated neurocognitive disorder in the context of HIV viral suppression in both blood and CSF. MATERIALS AND METHODS: Eighteen patients with active HIV-associated neurocognitive disorder (recent diagnosis with progressing symptoms) on combination antiretroviral therapy with viral suppression in both blood and CSF and 9 demographically matched control subjects underwent resting-state functional MR imaging. The connectivity in the 6 known neural networks was assessed. To localize significant ROIs within the HIV and control group, we performed a seed-based correlation for each known resting-state network. RESULTS: There were significant group differences between the control and HIV-associated neurocognitive disorder groups in the salience (0.26 versus 0.14, t = 2.6978, df = 25, P = .0123) and executive networks (0.52 versus 0.32, t = 2.2372, df = 25, P = .034). The covariate analysis with neuropsychological scores yielded statistically significant correlations in all 6 studied functional networks, with the most conspicuous correlation in salience networks. CONCLUSIONS: Active HIV-associated neurocognitive disorder in virally suppressed patients is associated with significantly decreased connectivity in the salience and executive networks, thereby making it potentially useful as a biomarker.
Authors: Roger C McIntosh; Robert Paul; Lishomwa C Ndhlovu; Melissa Hidalgo; Judith D Lobo; Maegen Walker; Cecilia M Shikuma; Kalpana J Kallianpur Journal: J Neurovirol Date: 2018-07-18 Impact factor: 2.643
Authors: Sheeba Arnold Anteraper; Kaundinya Gopinath; Michael J Hoch; Drenna Waldrop-Valverde; Donald Franklin; Scott L Letendre; Susan Whitfield-Gabrieli; Albert M Anderson Journal: J Neurovirol Date: 2021-03-05 Impact factor: 2.643
Authors: Shana A Hall; Zahra Lalee; Ryan P Bell; Sheri L Towe; Christina S Meade Journal: Prog Neuropsychopharmacol Biol Psychiatry Date: 2020-07-18 Impact factor: 5.067
Authors: Joanah Madzime; Martha Holmes; Mark F Cotton; Barbara Laughton; Andre J W van der Kouwe; Ernesta M Meintjes; Marcin Jankiewicz Journal: Brain Connect Date: 2021-08-23
Authors: Raha M Dastgheyb; Ned Sacktor; Donald Franklin; Scott Letendre; Thomas Marcotte; Robert Heaton; Igor Grant; Justin C McArthur; Leah H Rubin; Norman J Haughey Journal: J Acquir Immune Defic Syndr Date: 2019-09-01 Impact factor: 3.771